Seasonal variation in air particulate matter (PM10) exposure-induced ischemia-like injuries in the rat brain.

Epidemiological studies imply a significantly positive association between particulate matter (PM) level and ischemic stroke hospitalization. However, considering that PM10 is highly heterogeneous and varies with season within the same location, existing experimental evidence remained low. In the present study, we first treated Wistar rats with PM10 samples collected from different seasons in Taiyuan, a typically coal-burning city of China, and determined ischemia-related markers in the cortex.

[Epidemiology of rheumatoid arthritis in middle-aged and elderly population in Luohe City, Henan Province].

Objective: To explore the local prevalence of rheumatoid arthritis (RA) among the middle-aged and elderly population.

Methods: A total of 8610 residents were recruited for a two-stage cluster sampling survey through a questionnaire of RA according to 2010 ACR/EULAR classification criteria. Physical examinations and blood tests were performed.

Particulate matter (PM10) exposure induces endothelial dysfunction and inflammation in rat brain.

Epidemiological studies suggest that particulate matter (PM(10)) inhalation was associated with adverse effects on brain-related health, however, existing experimental data lacked relevant evidences. In this study, we treated Wistar rats with PM(10) at different concentrations (0.3, 1, 3 and 10 mg/kg body weight (bw)), and investigated endothelial dysfunction and inflammatory responses in the brain.

SO(2)-induced neurotoxicity is mediated by cyclooxygenases-2-derived prostaglandin E(2) and its downstream signaling pathway in rat hippocampal neurons.

Sulfur dioxide (SO(2)) pollution in atmospheric environment is involved in neurotoxicity and increased risk for hospitalization and mortality of many brain disorders; however, our understanding of the mechanisms by which SO(2) caused harmful insults on neurons remains elusive. Here, we show that SO(2) exposure produced a neuronal insult, and the neurotoxic effect was likely via stimulating cyclooxygenase-2 (COX-2) elevation by activation of nuclear factor-κB (NF-κB) activity and its acting on the promoter-distal NF-κB-binding site of COX-2 promoter. The action of SO(2) on elevating COX-2 ultimately appeared to be dependent on the increased production of arachidonic acid-derived prostaglandins, mainly prostaglandin E(2) (PGE(2)), and functioning of its EP2/4 receptors.

A highly efficient and selective turn-on fluorescent sensor for Cu2+ ion based on calix[4]arene bearing four iminoquinoline subunits on the upper rim.

A new fluorescent chemosensor based on calix[4]arene bearing four iminoquinoline subunits on the upper rim was conveniently synthesized, which showed a remarkable enhanced fluorescent intensity in the presence of Cu(2+) ion and a high selectivity toward Cu(2+) ion over a wide range of tested metal ions in acetonitrile.